The relationship of complement abnormalities to renal disease is under investigation. Purification, identification, metabolism and mechanism of action of the C3 nephritic factor is being attempted by studying patients with membranoproliferative glomerulonephritis and partial lipodystrophy. Fragments of C3, C3b, C3c, C3d and C3bi are being isolated from tryptic and KAF digests. The ultrastructure of the renal "zipper" in various pathologic conditions is being studied. The resistance of Forman rats to Heymann nephritis is being compared to the sensitivity of Lewis rats. The immunopathologic mechanism of this experimental nephritis is under investigation. BIBLIOGRAPHIC REFERENCES: Einstein, L.P., Alper, C.A., Bloch, K.J., Herrin, J.T., Rosen, F.S., David, J.R. and Colten, H.R. Biosynthetic defect in monocytes from human beings with genetic deficiency of the second component of complement. New Eng. J. Med. 292:1169-1171, 1975. Ziegler, J.B., Watson, L., Goodkofsky, I., Alper, C.A. and Lepow, I.H. Complement activation in semi-solid medium: insolubilization of properdin and the third component of complement (C3) in agar gels. J. Immunol. 116:75-79, 1976.